A Preliminary Formula to Predict Timing of Symptom Resolution for Collegiate Athletes Diagnosed With Sport Concussion

ContextSymptom presentation and recovery after sport concussion (SC) are variable. Empirically based models documenting typical symptom duration would assist health care providers in managing return to play after SC.ObjectiveTo develop a prediction model for SC symptom duration.DesignCross-sectional study.SettingTwo National Collegiate Athletic Association Division I university laboratories.Intervention(s)Participants completed the Revised Head Injury Scale (HIS-r), Immediate Post-Concussion Assessment and Cognitive Testing (ImPACT), and Sensory Organization Test within 24 hours of SC diagnosis.ResultsThe final formula consisted of the HIS-r''s self-reported neck pain, drowsiness, tingling, and nervousness duration and ImPACT total symptom severity (R = 0.62, R² = 39%, R²_adj = 34.2%, P < .001). Approximately 29% (R²_cv = 29%) of the variance associated with total days symptomatic after SC was explained by our preliminary formula when cross-validated. The current formula correctly identified 76% of participants who recovered within 10 days of injury.ConclusionsOur results suggest that self-reported duration of 4 symptoms during the initial 24 hours after injury along with total symptom severity as measured by ImPACT accounted for a considerable amount of variance associated with days symptomatic after SC in collegiate athletes. Until the formula is cross-validated in a college-aged sample, caution is warranted in using it clinically.Key Words: traumatic brain injuries, prediction, prolonged recovery, symptom severity, symptom duration

Key Points

• A formula to predict symptom resolution after sport concussion primarily consisting of initial symptom duration and severity correctly identified 76% of National Collegiate Athletic Association Division I collegiate athletes who recovered within 10 days.
• Before it can be used clinically, the formula must be cross-validated on larger samples.

The clinical presentation of and recovery from sport concussion (SC) are variable among athletes. Recovery curves based on animal models suggest the metabolic vulnerability associated with concussion resolves within approximately 7 to 10 days.^1,2 During this period of metabolic dysfunction, athletes experience neurocognitive and motor deficits as well as a constellation of symptoms.^3–5 These sequelae serve as markers that clinicians can measure to track recovery and make informed return-to-play and return-to-learn decisions.⁶The resolution of motor (eg, postural stability) and neurocognitive (eg, memory, reaction time, information-processing speed) deficits, along with self-reported symptoms (eg, headache, nausea, dizziness), varies based on a number of factors. These factors include age, sex, background history, comorbid conditions, and signs and symptoms reported or observed at the time of injury.^7–12 For example, in terms of age, only 50% of high school athletes (14–18 years of age) were reported to recover from SC in approximately 7 days, whereas 90% of adult athletes ≥18 years of age recovered in 7 days.^8,13–15 Regarding sex differences, Covassin et al¹⁶ observed that female high school athletes may take up to 14 days to recover in terms of memory and processing speed after concussion. In a separate study, Covassin et al¹² noted that concussed high school- and college-aged females consistently demonstrated higher symptom levels than male participants up to 14 days after concussion.Though the majority of concussion symptoms in older athletes resolve in ≤7 days of injury, approximately 10% of concussed athletes experience persistent symptoms up to 3 months after their diagnosis.¹⁷ Additionally, a subset of patients may experience 3 or more postconcussion symptoms for 3 months or longer, which is classified as postconcussion syndrome (PCS). Babcock et al¹⁸ found that 29% of pediatric concussion patients diagnosed in the emergency department for whom sport was the primary mechanism of injury (35%) were later diagnosed with PCS, which equates to 105 000 cases of pediatric PCS annually in the United States. The authors suggested that being able to prospectively identify candidates at risk for PCS would assist clinicians in discharge planning (eg, education, medications, and ongoing follow-up), ultimately resulting in improved patient outcomes.Studies examining predictors of SC recovery have usually addressed the dichotomy of typical recovery (7–13 days) versus protracted recovery.^3,12 Protracted recovery has been defined as resolution of SC lasting longer than 14,¹⁰ 21,¹¹ 45, or 90 days.^17,19 Several predictors, including loss of consciousness (LOC), posttraumatic amnesia (PTA), retrograde amnesia, total symptom severity, dizziness severity, and headache severity, have been associated with a 1.8- to 6-fold increase in risk for protracted recovery.^11,17,18 Of these predictors, LOC and amnesia are points of debate because of their infrequent occurrence and questionable relationship with injury severity and recovery.^8,11,20The objective of our study was to determine if the number of days an athlete reported concussion-related symptoms could be predicted from dependent variables derived from clinical measures commonly used to manage this injury. The ability to determine how many days an athlete will report SC-related symptoms may assist clinicians by allowing identification of athletes at risk for prolonged recoveries and institution of the appropriate medical and psychosocial infrastructure to assist in a full recovery.     

Bone disease in vitamin D-deficient patients with Crohn's disease

Vitamin D deficiency is frequently observed in patients with Crohn's disease and may be associated with an increased risk of development of metabolic bone disease. To estimate the incidence of metabolic bone disease by noninvasive methods, 31 patients (17–75 years old) with Crohn's disease and low 25-hydroxy vitamin D (25-OHD) levels in winter were investigated in the following summer by measuring the bone mineral content (BMC) of the distal radius by single photon absorptiometry and the cortical area ratio (CAR) calculated from radiographs of the right hand and by x-ray of the lumbar spine. Forty-five percent of the patients showed signs of metabolic bone disease. BMC and CAR correlated with 25-OHD serum levels (P<0.05), especially in men. Furthermore, the amount of sun exposure has an influence not only on 25-OHD serum levels both in summer and in winter (P=0.0006), but also on the BMC (P=0.07). Consequently, vitamin D deficiency is of major importance for the development of metabolic bone disease in patients with Crohn's disease. Vitamin D deficiency can be prevented by increasing sun exposure and long-term vitamin D supplementation.     

The folliculin-FNIP1 pathway deleted in human Birt-Hogg-Dube syndrome is required for murine B-cell development

Birt-Hogg-Dubé (BHD) syndrome is an autosomal dominant disorder characterized by cutaneous fibrofolliculomas, pulmonary cysts, and kidney malignancies. Affected individuals carry germ line mutations in folliculin (FLCN), a tumor suppressor gene that becomes biallelically inactivated in kidney tumors by second-hit mutations. Similar to other factors implicated in kidney cancer, FLCN has been shown to modulate activation of mammalian target of rapamycin (mTOR). However, its precise in vivo function is largely unknown because germ line deletion of Flcn results in early embryonic lethality in animal models. Here, we describe mice deficient in the newly characterized folliculin-interacting protein 1 (Fnip1). In contrast to Flcn, Fnip1(-/-) mice develop normally, are not susceptible to kidney neoplasia, but display a striking pro-B cell block that is entirely independent of mTOR activity. We show that this developmental arrest results from rapid caspase-induced pre-B cell death, and that a Bcl2 transgene reconstitutes mature B-cell populations, respectively. We also demonstrate that conditional deletion of Flcn recapitulates the pro-B cell arrest of Fnip1(-/-) mice. Our studies thus demonstrate that the FLCN-FNIP complex deregulated in BHD syndrome is absolutely required for B-cell differentiation, and that it functions through both mTOR-dependent and independent pathways.     

Rupture of the spleen following thoracoscopic spine surgery in a patient with chronic pancreatitis

Purpose

To highlight the perioperative risk of intracapsular haematoma of the spleen or splenic ruptures during thoracoscopic spine surgery in patients with chronic pancreatitis.

Methods

A 38-year-old patient with an L1 burst fracture (AO A3.3) underwent a standard thoracoscopic corpectomy and replacement of the vertebral body with an extendable vertebral body replacement 10 days after posterior instrumentation of T12–L2. In patients history chronic abusive alcoholism with related diseases such as pancreatitis, followed by hemipancreatectomy was found. Six hours after the surgery, the patient became hemodynamically unstable. An emergency CT scan revealed a splenic rupture. Emergent splenectomy was performed.

Results

After surgical treatment of the L1 burst fracture, a rupture of the spleen was detected. An immediate splenectomy was performed. At the 18-month follow-up, an unchanged stable position of the cage was observed on CT.

Conclusions

Due to its proximity to the thoracolumbar junction, the spleen is vulnerable to injury during spine surgery. If the patient has undergone previous intra-abdominal operations or chronic inflammation of the pancreas is found, special care of the spleen during the operation is necessary.

     

Treatment strategies for infection after reverse shoulder arthroplasty

Introduction

Infection after reverse shoulder arthroplasty (RSA) is a disastrous complication. No clear guidelines describing specific management strategies for infection after RSA are available.

Methods

We retrospectively analyzed 20 patients treated for deep infection after RSA. Initial irrigation and debridement and exchange of the polyethylene inlay were performed in seven patients, and initial two-stage revision was performed in 12 and initial resection arthroplasty in one patient. Patient charts were reviewed for risk factors, clinical symptoms and investigations of those symptoms, pre- and postoperative X-rays, interval until revision surgery, causative bacteria, complications, final clinical outcome and patient satisfaction.

Results

The mean overall postoperative Constant–Murley Score (CMS) was 42.6 points, the mean UCLA score was 20.8, the mean simple shoulder test (SST) was 5.5, and the mean VAS was 1.5. When comparing the CMS, UCLA score and the SST between the revision RSA group and the resection group, significant differences between the groups were found (p < 0.05). Irrigation, debridement and exchange of the polyethylene inlay were successful only in two of the four patients with acute infection. The three patients with subacute infections were treated with initial irrigation and debridement and exchange of the polyethylene inlay, which were not successful.

Conclusion

The relatively high patient satisfaction can be explained by the low pain level once the patient is free from infection. However, functional results are poor in most cases, and this possible outcome must be discussed with the patient in the preoperative setting.     

Lytic effector cell function in schizophrenia and depression

Natural killer (NK) cell activity and antibody-dependent cellular cytotoxicity (ADCC) were tested in patients with schizophrenia or depression. It was found that NK activity as well as ADCC were significantly lower in both groups, as compared to healthy control individuals (P less than 0.001). Psychopharmacologic treatment with neuroleptics and antidepressives resulted in a significant increase in NK activity and ADCC (P less than 0.005) in patients with schizophrenia but not in treated patients with depression. In patients with schizophrenia, no correlation could be established between the dose of neuroleptic given and the increase in NK activity. Lithium also did not produce an increase in NK activity and ADCC. The addition of serum, derived from untreated patients with schizophrenia, to cell cultures in concentrations of 10 and 20% had an inhibitory effect upon the ADCC and, to a lesser degree, upon NK activity (20% serum concentration only); sera from treatment schizophrenics produced no inhibition of NK activity, but did affect ADCC. No serum-derived inhibitory effect upon either NK activity or ADCC was found to be present in sera from patients with depression. We conclude that lytic effector mechanisms are impaired in patients with schizophrenia or depression and that this defect is reversed in schizophrenic patients on treatment, but not in depressives on therapy. Patients with schizophrenia also tend to have a reversible serum-mediated inhibition of NK activity which is absent in patients with depression.     

Interleukin 1 induces specific phosphorylation of a 41 kDa plasma membrane protein from the human tumor cell line K 562

An in vitro system was established to investigate the early effects of interleukin 1 (IL 1) on a clearly defined subcellular system, the plasma membrane. Murine IL 1 was obtained from the macrophage tumor line P 388 D1 and purified to apparent homogeneity. Plasma membranes from the human leukaemic tumor cell line K 562 were highly purified by differential ultracentrifugation. The monokine induced the specific phosphorylation of a 41 kDa plasma membrane protein. This could be demonstrated by incubating the plasma membranes in the presence of IL 1 and (gamma-32P)-ATP, separating the proteins by SDS-PAGE and subsequent autoradiography. A first biochemical reaction caused by IL 1 in the target organelle of the cell, the plasma membrane, was discovered, yielding a clue of how signal transmission may take place finally resulting in the stimulation of the responding cell.